Practice question

Developmental plasticity allows endocrine disruptors to epigenetically program hormone responsiveness. Transient prenatal exposure to DES or BPA induces persistent hypomethylation of estrogen receptor promoters and histone acetylation changes in target tissues such as uterus, breast, prostate, increasing receptor expression. Upon endogenous hormone surge at puberty, primed tissues exhibit exaggerated proliferative response, hypersensitivity to estrogen or androgen, leading to hyperplasia and tumor predisposition. Instead of becoming resistant, tissues become more sensitive to hormones later in life, explaining why low-dose fetal exposures amplify adult hormonal responses and increase disease susceptibility.